Astaxanthin inhibits tumor invasion by decreasing extracellular matrix production and induces apoptosis in experimental rat colon carcinogenesis by modulating the expressions of ERK-2, NFkB and COX-2

2009 ◽  
Vol 29 (2) ◽  
pp. 207-224 ◽  
Author(s):  
Ponnuraj Nagendraprabhu ◽  
Ganapasam Sudhandiran
Keyword(s):  
Extracellular Matrix ◽  
Tumor Invasion ◽  
Colon Carcinogenesis ◽  
Rat Colon ◽  
Extracellular Matrix Production ◽  
Matrix Production ◽  
Cox 2

Effect of HMG-CoA Reductase Inhibition on Vascular Smooth Muscle Cells Extracellular Matrix Production: Role of RhoA

2016 ◽  
Vol 14 (4) ◽  
pp. 345-352 ◽  
Author(s):  
Rogelio Palomino-Morales ◽  
Sonia Perales ◽  
Carolina Torres ◽  
Ana Linares ◽  
Maria J. Alejandre
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Extracellular Matrix Production ◽  
Matrix Production ◽  
Coa Reductase

Dynamics of extracellular matrix production and turnover in tissue engineered cardiovascular structures

2001 ◽  
Vol 81 (2) ◽  
pp. 220-228 ◽  
Author(s):  
Ulrich A. Stock ◽  
Dmitri Wiederschain ◽  
Susan M. Kilroy ◽  
Dominique Shum-Tim ◽  
Philip N. Khalil ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Extracellular Matrix Production ◽  
Matrix Production

Glucosamine sulphate does not increase extracellular matrix production at low oxygen tension

2009 ◽  
Vol 337 (1) ◽  
pp. 103-111 ◽  
Author(s):  
Cheng-Juan Qu ◽  
Teemu Pöytäkangas ◽  
Marjo Jauhiainen ◽  
Seppo Auriola ◽  
Mikko J. Lammi
Keyword(s):  
Extracellular Matrix ◽  
Oxygen Tension ◽  
Low Oxygen ◽  
Low Oxygen Tension ◽  
Extracellular Matrix Production ◽  
Glucosamine Sulphate ◽  
Matrix Production

The influence of oxygen concentration on the extracellular matrix production of human nucleus pulposus cells during isolation-expansion process

2017 ◽  
Vol 105 (6) ◽  
pp. 1575-1582 ◽  
Author(s):  
Shu-Hua Yang ◽  
Ming-Hsiao Hu ◽  
Wan-Yu Lo ◽  
Yuan-Hui Sun ◽  
Chang-Chin Wu ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Nucleus Pulposus ◽  
Oxygen Concentration ◽  
Nucleus Pulposus Cells ◽  
Expansion Process ◽  
Extracellular Matrix Production ◽  
Matrix Production

scholarly journals Laminin-5 activates extracellular matrix production and osteogenic gene focusing in human mesenchymal stem cells

2007 ◽  
Vol 26 (2) ◽  
pp. 106-114 ◽  
Author(s):  
Robert F. Klees ◽  
Roman M. Salasznyk ◽  
Scott Vandenberg ◽  
Kristin Bennett ◽  
George E. Plopper
Keyword(s):  
Stem Cells ◽  
Extracellular Matrix ◽  
Mesenchymal Stem Cells ◽  
Human Mesenchymal Stem Cells ◽  
Laminin 5 ◽  
Extracellular Matrix Production ◽  
Matrix Production ◽  
Osteogenic Gene

scholarly journals Differentiation of cardiomyocytes from human embryonic stem cells is accompanied by changes in the extracellular matrix production of versican and hyaluronan

2010 ◽  
Vol 111 (3) ◽  
pp. 585-596 ◽  
Author(s):  
Christina K. Chan ◽  
Marsha W. Rolle ◽  
Susan Potter-Perigo ◽  
Kathleen R. Braun ◽  
Benjamin P. Van Biber ◽  
...  
Keyword(s):  
Stem Cells ◽  
Extracellular Matrix ◽  
Embryonic Stem Cells ◽  
Human Embryonic Stem Cells ◽  
Embryonic Stem ◽  
Extracellular Matrix Production ◽  
Matrix Production

Targeting ER protein TXNDC5 in hepatic stellate cell mitigates liver fibrosis by repressing non-canonical TGFβ signalling

Gut ◽  
2021 ◽  
pp. gutjnl-2021-325065
Author(s):  
Chen-Ting Hung ◽  
Tung-Hung Su ◽  
Yen-Ting Chen ◽  
Yueh-Feng Wu ◽  
You-Tzung Chen ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Transforming Growth Factor ◽  
Stellate Cell ◽  
Transforming Growth Factor Β1 ◽  
Duct Ligation ◽  
Extracellular Matrix Production ◽  
Matrix Production

Background and objectivesLiver fibrosis (LF) occurs following chronic liver injuries. Currently, there is no effective therapy for LF. Recently, we identified thioredoxin domain containing 5 (TXNDC5), an ER protein disulfide isomerase (PDI), as a critical mediator of cardiac and lung fibrosis. We aimed to determine if TXNDC5 also contributes to LF and its potential as a therapeutic target for LF.DesignHistological and transcriptome analyses on human cirrhotic livers were performed. Col1a1-GFPTg, Alb-Cre;Rosa26-tdTomato and Tie2-Cre/ERT2;Rosa26-tdTomato mice were used to determine the cell type(s) where TXNDC5 was induced following liver injury. In vitro investigations were conducted in human hepatic stellate cells (HSCs). Col1a2-Cre/ERT2;Txndc5fl/fl (Txndc5cKO) and Alb-Cre;Txndc5fl/fl (Txndc5Hep-cKO) mice were generated to delete TXNDC5 in HSCs and hepatocytes, respectively. Carbon tetrachloride treatment and bile duct ligation surgery were employed to induce liver injury/fibrosis in mice. The extent of LF was quantified using histological, imaging and biochemical analyses.ResultsTXNDC5 was upregulated markedly in human and mouse fibrotic livers, particularly in activated HSC at the fibrotic foci. TXNDC5 was induced by transforming growth factor β1 (TGFβ1) in HSCs and it was both required and sufficient for the activation, proliferation, survival and extracellular matrix production of HSC. Mechanistically, TGFβ1 induces TXNDC5 expression through increased ER stress and ATF6-mediated transcriptional regulation. In addition, TXNDC5 promotes LF by redox-dependent JNK and signal transducer and activator of transcription 3 activation in HSCs through its PDI activity, activating HSCs and making them resistant to apoptosis. HSC-specific deletion of Txndc5 reverted established LF in mice.ConclusionsER protein TXNDC5 promotes LF through redox-dependent HSC activation, proliferation and excessive extracellular matrix production. Targeting TXNDC5, therefore, could be a potential novel therapeutic strategy to ameliorate LF.

scholarly journals Role of the Autotaxin-LPA Pathway in Dexamethasone-Induced Fibrotic Responses and Extracellular Matrix Production in Human Trabecular Meshwork Cells

2018 ◽  
Vol 59 (1) ◽  
pp. 21 ◽  
Author(s):  
Megumi Honjo ◽  
Nozomi Igarashi ◽  
Junko Nishida ◽  
Makoto Kurano ◽  
Yutaka Yatomi ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Trabecular Meshwork ◽  
Trabecular Meshwork Cells ◽  
Extracellular Matrix Production ◽  
Matrix Production

scholarly journals Amplified canonical transforming growth factor-β signalling via heat shock protein 90 in pulmonary fibrosis

2016 ◽  
Vol 49 (2) ◽  
pp. 1501941 ◽  
Author(s):  
Zaneta Sibinska ◽  
Xia Tian ◽  
Martina Korfei ◽  
Baktybek Kojonazarov ◽  
Janina Susanne Kolb ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Growth Factor ◽  
Pulmonary Fibrosis ◽  
Transforming Growth Factor ◽  
A549 Cells ◽  
Lung Fibroblasts ◽  
Hsp90 Inhibition ◽  
Extracellular Matrix Production ◽  
Matrix Production ◽  
Β Receptor

Interstitial lung fibroblast activation coupled with extracellular matrix production is a pathological signature of idiopathic pulmonary fibrosis (IPF), and is governed by transforming growth factor (TGF)-β/Smad signalling. We sought to define the role of heat shock protein (HSP)90 in profibrotic responses in IPF and to determine the therapeutic effects of HSP90 inhibition in a murine model of pulmonary fibrosis.We investigated the effects of HSP90 inhibition in vitro by applying 17-AAG (17-allylamino-17-demethoxygeldanamycin) to lung fibroblasts and A549 cells and in vivo by administering 17-DMAG (17-dimethylaminoethylamino-17-demethoxygeldanamycin) to mice with bleomycin-induced pulmonary fibrosis.HSP90 expression was increased in (myo)fibroblasts from fibrotic human and mouse lungs compared with controls. 17-AAG inhibited TGF-β1-induced extracellular matrix production and transdifferentiation of lung fibroblasts and epithelial–mesenchymal transition of A549 cells. The antifibrotic effects were associated with TGF-β receptor disruption and inhibition of Smad2/3 activation. Co-immunoprecipitation revealed that HSP90β interacted with TGF-β receptor II and stabilised TGF-β receptors. Furthermore, 17-DMAG improved lung function and decreased fibrosis and matrix metalloproteinase activity in the lungs of bleomycin-challenged mice.In conclusion, this is the first study to demonstrate that HSP90 inhibition blocks pulmonary fibroblast activation and ameliorates bleomycin-induced pulmonary fibrosis in mice.

Sign in / Sign up

Export Citation Format

Share Document